Since others and we have shown that BM-MSC PKC activity is partially responsible for the BM-MSC supportive role and drug resistance in various haematological malignancies [40,41], and because PKC activity is carried out upstream of NF-κB [42], here we have studied the effect of inhibiting these connected signalling molecules in BM-MSC on the sensitivity of MM cells to BTZ treatment. The gene discussed is PRRT2; the disease is Miyoshi myopathy.